Marc Joseph Nutrition - Blog

A couple of more studies just released that again suggest omega fatty acids may be helpful in slowing cognitive decline:

Omega-3 fatty acid treatment in 174 patients with mild to moderate Alzheimer disease

This study found that patients with very mild Alzheimer’s disease (AD) who supplemented with omega-3 fatty acids (2.3 g/day)experienced significantly slower rates of decline in mental function. However, individuals with mild to moderate AD didn’t improve.

This result reinforces the importance of early intervention and prevention. Once damage to the brain is significant (as seen in moderate cases of AD), a single helpful nutrient like omega-3 fats, although not detrimental, is likely to not necessarily lead to great improvement.

Dietary supplementation of arachidonic and docosahexaenoic acids improves cognitive dysfunction.

Arachidonic acid is an omega-6 fat, while docosahexaenoic acid (or DHA) is an omega-3 fat. Most people get plenty of omega-6 fats in the diet, as they are found in high quantities in vegetable oils used in processed and restaurant-prepared foods. Arachidonic acid (ARA) is also found in high amounts in red meat and egg yolks. On the other hand, most people are deficient in omega-3 fats, such as DHA and eicosapentaenoic acid (EPA), which are found in fish oil.

This second study found that individuals with mild cognitive impairment who supplemented with only 240 mg of ARA and DHA experienced improvements in both immediate memory and attention scores. As in the earlier study, no improvement was seen in individuals who had already developed AD.

For omega-3 fats DHA & EPA, it’s important to make sure that the source (fish or supplements) is low in contaminants, such as heavy metals and PCBs. Tested fish oil supplements are your best bet there.

You can learn more about the important roles of omega-3 fats in disease prevention and treatment here.

And, you can learn more about ways to preserve and improve cognitive function here.

Researchers at the Mayo Clinic’s Molecular Neuroscience Program recently published research that suggests common picornaviruses, including rhinoviruses (e.g., common cold) and enteroviruses, may infect the brain and lead to ongoing damage to areas of the brain involving memory.

The study was an animal study that infected mice with Theiler’s encephalomyelitis virus, which is an enterovirus similar to the human polio virus. Mice were then tested using a maze test. Some mice were not affected much at all, while others had great difficulty in navigating the maze. When researchers dissected the mice, they found that the performance on the test directly correlated to the amount of viral damage to the hippocampus, which is the brain structure primarily responsible for learning and memory.

The researchers hypothesize that some cases of human cognitive impairment and memory loss may be the result of the cumulative effect of multiple viral infections over the course of one’s lifetime.

Obviously, more research remains to be done to prove this hypothesis, but the general idea of reducing one’s viral load is a good one. Both prescription drugs (e.g., Valtrex) and natural substances (e.g., olive leaf extract) can be very effective in doing just that.

Curcumin, the yellow pigment found in tumeric, a common ingredient in curry, may help to protect against cognitive decline and slow the development of Alzheimer’s disease (AD).

There’s been quite a bit of research done the past few years regarding the potential connection. Two recent studies reinforce that link.

The first study looked cognitive performance and curry consumption in older, non-demented Asian individuals (aged 60-93 years). Researchers found that those who ate curry occasionally or frequently scored significantly better on a standardized mental health test. Those people who consumed curry often or very frequently had a 49% reduced risk of cognitive impairment, while those consuming it occasionally had a 38% decreased risk.

The study was observational, so cause and effect could not be determined (there may have been other factors playing a role — e.g., vegetable and fat intake), but the results are consistent with earlier experimental evidence on curry.

The second recent study found that immune system cells (macrophages) in blood drawn from AD patients were able to break down beta-amyloid plaques (found in the brains of AD patients) significantly better when treated with curcumin.

This study was a lab study (i.e., the test were done on the blood samples in petri dishes), but nevertheless the results were consistent with earlier research examining the effects of curcumin on immune system function.

Finally, this review study provides a good overview of curcumin’s suspected biochemical benefits in diseases such as AD, as well as for other conditions, such as cancer, heart disease, inflammatory digestive disorders, arthritis, and osteoporosis. In short, curcumin seems to have an excellent ability to regulate proteins, enzymes, and other factors that manage immune system response.

Curcumin certainly seems like a safe and important substance to potentially help prevent and treat many chronic conditions.

(Note: If you’re considering increasing tumeric intake by eating restaurant prepared curries, it’s important to consider the type and and amounts of fats used in their preparation. Restaurant-prepared curries can often be high in fats, especially saturated fats (like ghee, or clarified butter, and vegetable oil). In high amounts, these fats may counteract some of the curry’s beneficial effects by promoting elevated cholesterol and/or inflammation. Try to identify restaurants that use moderate amounts of these fats and/or other more healthy alternatives, such as olive oil.)

Calorie-restriction has been highlighted as a way to slow the aging process in general. Recent research looks at the potential for calorie-restriction to slow the progression of Alzheimer’s Disease (AD).

The researchers fed mice bred to develop AD a reduced-calorie diet (mostly through the reduction of carbohydrate intake), and found that the mice had fewer disease symptoms and better memories than the control group fed a regular-calorie diet.

In a separate study, the same researchers applied SIRT1, one of the sirtuin proteins with increased expression seen in calorie restriction and believed to play an important role in slowing aging, into the nerve cells affected by AD. They found that SIRT1 helped to prevent the cleavage of beta-amyloid precursor molecules, which, in turn, slowed the formation of plaques.

So, calorie-restriction (with adequate nutrition) may be one way to help slow the progression of aging and cognitive decline. Other potential approaches to preserving cognitive function are discussed here.